Grace Oscullo1, E Sapiña-Beltrán2,3, Gerard Torres2,3, Enrique Zaldivar1, Ferran Barbé2,3, Miguel Angel Martinez-Garcia4. 1. Pneumology Department, Hospital Universitario y Politécnico La Fe, Bulevar Sur s/n, 46012, Valencia, Spain. 2. Group of Translational Research in Respiratory Medicine, IRBLleida, Hospital Universitari Arnau de Vilanova and Santa Maria, Lleida, Cataluña, Spain. 3. Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), Madrid, Spain. 4. Pneumology Department, Hospital Universitario y Politécnico La Fe, Bulevar Sur s/n, 46012, Valencia, Spain. mianmartinezgarcia@gmail.com.
Abstract
PURPOSE OF REVIEW: This review seeks to present an overview of the recently found association between refractory hypertension (RfH) and obstructive sleep apnoea (OSA). RECENT FINDINGS: RfH was recently defined as an extreme phenotype of resistant hypertension characterized by the lack of blood pressure control despite using ≥ 5 antihypertensive drugs at optimal doses. Current data support that the pathophysiological pathway of both types of hypertension is different. The main mechanism involved in resistant hypertension is fluid retention whereas in the case of RfH is the sympathetic over-activity. OSA is now recognized as a cause of hypertension (especially in the case of difficult-to-treat hypertension). It seems that the biological mechanism linking OSA and arterial hypertension is the sympathetic over-activity related to the respiratory events (apnoeas and hypopnoeas) during the night. So, it is not surprising that, although the literature is scarce, some studies have found a very high prevalence of OSA and an excess of sympathetic activity in patients with RfH. Finally, a very recent study demonstrated that continuous positive airway pressure (CPAP) treatment, which controls sympathetic activation in OSA patients, achieves very significant reductions in blood pressure levels in RfH patients, even greater than in those with resistant (non-refractory) hypertension. The prevalence of OSA in patients with RfH is very high. CPAP treatment achieves a clinically significant reduction in blood pressure levels in those patients with RfH (especially in night readings). Patients with RfH must be sent to a sleep unit for a study.
PURPOSE OF REVIEW: This review seeks to present an overview of the recently found association between refractory hypertension (RfH) and obstructive sleep apnoea (OSA). RECENT FINDINGS: RfH was recently defined as an extreme phenotype of resistant hypertension characterized by the lack of blood pressure control despite using ≥ 5 antihypertensive drugs at optimal doses. Current data support that the pathophysiological pathway of both types of hypertension is different. The main mechanism involved in resistant hypertension is fluid retention whereas in the case of RfH is the sympathetic over-activity. OSA is now recognized as a cause of hypertension (especially in the case of difficult-to-treat hypertension). It seems that the biological mechanism linking OSA and arterial hypertension is the sympathetic over-activity related to the respiratory events (apnoeas and hypopnoeas) during the night. So, it is not surprising that, although the literature is scarce, some studies have found a very high prevalence of OSA and an excess of sympathetic activity in patients with RfH. Finally, a very recent study demonstrated that continuous positive airway pressure (CPAP) treatment, which controls sympathetic activation in OSA patients, achieves very significant reductions in blood pressure levels in RfH patients, even greater than in those with resistant (non-refractory) hypertension. The prevalence of OSA in patients with RfH is very high. CPAP treatment achieves a clinically significant reduction in blood pressure levels in those patients with RfH (especially in night readings). Patients with RfH must be sent to a sleep unit for a study.
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